ReviewLeukemia2015
Role of chromosomal aberrations in clonal diversity and progression of acute myeloid leukemia.
Review in Leukemia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- Clonal Evolution in 207 Cases of Refractory or Relapsed Acute Myeloid Leukemia.European journal of haematology · 2025Article
- Proteomic Characterization of Acute Myeloid Leukemia for Precision Medicine.Molecular & cellular proteomics : MCP · 2023Review
- Circular RNAs Activity in the Leukemic Bone Marrow Microenvironment.Non-coding RNA · 2022Review
- Prognostic impact of chromosomal changes at relapse after allogeneic hematopoietic cell transplantation for acute myeloid leukemia or myelodysplastic syndrome.Bone marrow transplantation · 2022Article
- Polymorphism of VDR Gene and the Sensitivity of Human Leukemia and Lymphoma Cells to Active Forms of Vitamin D.Cancers · 2022Article
- Review
- Chromosomal Instability in Acute Myeloid Leukemia.Cancers · 2021Review
- Pre-HCT mosaicism increases relapse risk and lowers survival in acute lymphoblastic leukemia patients post-unrelated HCT.Blood advances · 2021Article
- Targeting multiple signaling pathways: the new approach to acute myeloid leukemia therapy.Signal transduction and targeted therapy · 2020Review
- Immunotherapy for acute myeloid leukemia: from allogeneic stem cell transplant to novel therapeutics.Leukemia & lymphoma · 2019Review
- Article
- Review
- Nonclonal chromosomal alterations and poor survival in cytopenic patients without hematological malignancies.Molecular cytogenetics · 2019Article
- DEAD-box helicase 27 plays a tumor-promoter role by regulating the stem cell-like activity of human colorectal cancer cells.OncoTargets and therapy · 2019Article
- Neuroblastoma with flat genomic profile: a question of representativity?BMJ case reports · 2018Article
- Chromosomal abnormality variation detected by G-banding is associated with prognosis of diffuse large B-cell lymphoma treated by R-CHOP-based therapy.Cancer medicine · 2018Article
- SEECancer: a resource for somatic events in evolution of cancer genome.Nucleic acids research · 2018Article
- PARP3 is a promoter of chromosomal rearrangements and limits G4 DNA.Nature communications · 2017Article
- The genetics of myelodysplastic syndrome: from clonal haematopoiesis to secondary leukaemia.Nature reviews. Cancer · 2017Review
- Genomic and transcriptomic profiling of resistant CEM/ADR-5000 and sensitive CCRF-CEM leukaemia cells for unravelling the full complexity of multi-factorial multidrug resistance.Scientific reports · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genetic abnormalities are a hallmark of cancer. Hereby, cytogenetic aberrations and small-scale abnormalities, such as single-nucleotide variations and insertion/deletion mutations, have emerged as two alternative modes of genetic diversification. Both mechanisms are at work in acute myeloid leukemia (AML), in which conventional karyotyping and molecular studies demonstrate that gene mutations occur predominantly in cytogenetically normal AML, whereas chromosomal changes are a driving force of development and progression of disease in aberrant karyotype AML. All steps of disease evolution in AML, ranging from the transformation of preleukemic clones into overt leukemia to the expansion and recurrence of malignant clones, are paralleled by clonal evolution at either the gene mutation or chromosome aberration level. Preleukemic conditions, such as Fanconi anemia and Bloom syndrome, demonstrate that the acquisition of chromosomal aberrations can contribute to leukemic transformation. Similar to what has been shown at the mutational level, expansion and recurrence of AML clones goes along with increasing genetic diversification. Hereby, cytogenetically more evolved subclones are at a proliferative advantage and outgrow ancestor clones or have evolved toward a more aggressive behavior with additional newly acquired aberrations as compared with the initial leukemic clone, respectively.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.